The Role of ncRNAs in the Immune Dysregulation of Preeclampsia

Int J Mol Sci. 2023 Oct 16;24(20):15215. doi: 10.3390/ijms242015215.

Abstract

The main complications causing practically 75% of all maternal deaths are severe bleeding, infections, and high blood pressure during pregnancy (preeclampsia (PE) and eclampsia). The usefulness of ncRNAs as clinical biomarkers has been explored in an extensive range of human diseases including pregnancy-related diseases such as PE. Immunological dysregulation show that the Th1/17:Th2/Treg ratio is "central and causal" to PE. However, there is evidence of the involvement of placenta-expressed miRNAs and lncRNAs in the immunological regulation of crucial processes of placenta development and function during pregnancy. Abnormal expression of these molecules is related to immune physiopathological processes that occur in PE. Therefore, this work aims to describe the importance of miRNAs and lncRNAs in immune dysregulation in PE. Interestingly, multiple ncRNAS are involved in the immune dysregulation of PE participating in type 1 immune response regulation, immune microenvironment regulation in placenta promoting inflammatory factors, trophoblast cell invasion in women with Early-Onset PE (EOPE), placental development, and angiogenesis, promotion of population of M1 and M2, proliferation, invasion, and migration of placental trophoblast cells, and promotion of invasion and autophagy through vias such as PI3K/AKT/mTOR, VEGF/VEGFR1, and TLR9/STAT3.

Keywords: LncRNA; immune dysregulation; miRNA; ncRNA; preeclampsia; pregnancy.

Publication types

  • Review

MeSH terms

  • Female
  • Humans
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Placenta / metabolism
  • Pre-Eclampsia* / metabolism
  • Pregnancy
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Trophoblasts / metabolism

Substances

  • Phosphatidylinositol 3-Kinases
  • RNA, Long Noncoding
  • MicroRNAs

Grants and funding

This research received no funding.